[Crucial roles of Helicobacter pylori infection in the pathogenesis of gastric cancer and gastric mucosa-associated lymphoid tissue (MALT) lymphoma].

Helicobacter pylori (H. pylori) is a gram-negative helical rod that colonizes human gastric mucosa. Its discovery has opened up new opportunities regarding the understating and management of gastrointestinal disorders. In humans, infection with H. pylori has been established as a major cause of chronic gastritis and peptic ulcer, and is important in the pathogenesis of gastric cancer and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Bacterial and host factors determine the outcome of H. pylori infection. The eradication of H. pylori can, therefore, contribute to the treatment and prevention of these diseases. H. pylori infection plays a critical role in gastric carcinogenesis through two major pathways: the indirect action of H. pylori on gastric epithelial cells through inflammation, and the direct action of the bacteria on epithelial cells through the induction of protein modulation and gene mutation. MALT lymphoma is a common low grade B-cell lymphoma arising from a background of chronic inflammatory disease at a number of mucosal sites. Those originating in the stomach are causatively linked to H. pylori infection, and eradication of the bacterium with antibiotics leads to the long-term complete regression of lymphoma. t (11;18)/API2-MALT1 and t(1;14)/IGH-BCL10 are specifically associated with the gastric MALT lymphoma entity, and the oncogenic products of these translocations have been shown to target a common molecular pathway, i.e., the nuclear factor-kappaB pathway. This paper reviews recent advances in our understanding of the association of H. pylori infection with gastric cancer and gastric MALT lymphoma and the molecular genetics underlying tumor development.